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Updated: May 11, 2026

11:56
Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
Published on: August 24, 2015
CD134 is a cellular receptor specific for human herpesvirus-6B entry
Huamin Tang1, Satoshi Serada, Akiko Kawabata
1Division of Clinical Virology, Center for Infectious Diseases, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Summary
Human herpesvirus-6B (HHV-6B) uses CD134 as its specific entry receptor, unlike HHV-6A. This discovery clarifies HHV-6B
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Human herpesvirus-6B (HHV-6B) is a distinct species of beta-herpesvirus.
- HHV-6B establishes lifelong latent infections after childhood primary infection, causing exanthem subitum and potential severe complications.
- Reactivation of HHV-6B in immunosuppressed individuals can lead to encephalitis.
Purpose of the Study:
- To identify the specific cellular entry receptor for Human herpesvirus-6B (HHV-6B).
- To elucidate the mechanism of HHV-6B cellular entry and its interaction with host factors.
Main Methods:
- Utilized T-cell lines with varying CD134 expression levels to assess HHV-6B permissiveness.
- Investigated the interaction between soluble CD134 and HHV-6B viral glycoproteins.
- Analyzed CD134 expression levels in HHV-6B-infected T cells.
Main Results:
- CD134, a TNF receptor superfamily member, was identified as the specific entry receptor for HHV-6B.
- Overexpression of CD134 rendered normally nonpermissive T cells susceptible to HHV-6B infection.
- Soluble CD134 inhibited HHV-6B infection by interacting with viral glycoproteins, but did not affect HHV-6A.
- CD134 expression was downregulated upon HHV-6B infection.
Conclusions:
- CD134 is the specific cellular receptor mediating HHV-6B entry into T cells.
- Understanding CD134's role provides critical insights into HHV-6B pathogenesis and viral entry mechanisms.
- This finding differentiates HHV-6B entry from HHV-6A, which uses CD46.
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